Vitamin D3 Inhibits Helicobacter pylori Infection by Activating the VitD3/VDR-CAMP Pathway in Mice

Zhou, Anni; Li, Lei; Zhao, Guiping; Min, Li; Liu, Si; Zhu, Shengtao; Guo, Qingdong; Liu, Chunjie; Zhang, Shutian

doi:10.3389/fcimb.2020.566730

Cited by 20 publications

(16 citation statements)

References 44 publications

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“…Vitamin D3 stimulates innate immune antibacterial activity in several cell types through increase in the production of antimicrobial factors [ 111 ]. Accordingly, two different studies concluded that supplementation with vitamin D3 at different doses, for 14 days or 2 months, and treatment with vitamin D3 for 72 h in human normal gastric epithelial cells HFE145 led to H. pylori eradication [ 110 , 111 ]. The study conducted by Hu et al demonstrated that H. pylori infection affected Ca 2+ release from lysosomes of epithelial gastric cells, disrupting lysosomal acidification and allowing the bacteria to remain in the lysosomes.…”

Section: Management Of Helicobacter Pylori Infectionmentioning

confidence: 99%

“…They suggested that vitamin D3 exerted its bactericidal properties by enhancing the lysosomal degradation function via the PDIA3-STAT3-MCOLN3-Ca 2+ axis [ 111 ]. In contrast, Zhou et al proposed a mechanism wherein vitamin D3 increased the expression of the vitamin D receptor (VDR) and cathelicidin antimicrobial peptides (CAMPs) in the gastric mucosa by binding of the vitamin D3 and VDR complex to the CAMPs promoter [ 110 ].…”

Section: Management Of Helicobacter Pylori Infectionmentioning

confidence: 99%

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Impact of Dietary Patterns on H. pylori Infection and the Modulation of Microbiota to Counteract Its Effect. A Narrative Review

et al. 2021

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Helicobacter pylori (H. pylori) is a Gram-negative bacterium that colonizes the stomach and can induce gastric disease and intra-gastric lesions, including chronic gastritis, peptic ulcers, gastric adenocarcinoma, and mucosa-associated lymphoid tissue lymphoma. This bacterium is responsible for long-term complications of gastric disease. The conjunction of host genetics, immune response, bacterial virulence expression, diet, micronutrient availability, and microbiome structure influence the disease outcomes related to chronic H. pylori infection. In this regard, the consumption of unhealthy and unbalanced diets can induce microbial dysbiosis, which infection with H. pylori may contribute to. However, to date, clinical trials have reported controversial results and current knowledge in this field is inconclusive. Here, we review preclinical studies concerning the changes produced in the microbiota that may be related to H. pylori infection, as well as the involvement of diet. We summarize and discuss the last approaches based on the modulation of the microbiota to improve the negative impact of H. pylori infection and their potential translation from bench to bedside.

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Section: Management Of Helicobacter Pylori Infectionmentioning

confidence: 99%

Section: Management Of Helicobacter Pylori Infectionmentioning

confidence: 99%

Impact of Dietary Patterns on H. pylori Infection and the Modulation of Microbiota to Counteract Its Effect. A Narrative Review

et al. 2021

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“…The active form of vitamin D 3 (VitD 3 ) is 1α,25-(OH) 2 -D 3 , which forms 25-hydroxyvitamin D 3 under the catalysis of 25-hydroxylase in the liver and further forms 1α,25-(OH) 2 -D 3 through the action of 1-α hydroxylase in the kidney [1]. VitD 3 is a fat-soluble vitamin type that plays an important role in many physiological processes related to human health; the lack of VitD 3 would inhibit the absorption of calcium and phosphorus in the small intestine and cause the reduction of bone mineral density, which increases the risk of fracture [2].…”

Section: Introductionmentioning

confidence: 99%

Vitamin D3 Protects Mice from Diquat-Induced Oxidative Stress through the NF-κB/Nrf2/HO-1 Signaling Pathway

Zhang

Liu

Fang

et al. 2021

Oxidative Medicine and Cellular Longevity

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Vitamin D3, as an indispensable and fat-soluble micronutrient, plays an important role in the health of humans and animals. At present, studies are focusing on the calcium absorption and immunoregulation function of vitamin D3; this study was aimed at exploring the antioxidative stress ability of vitamin D3 on diquat-induced intestinal dysfunction of ICR mice and the underlying mechanism. The results showed that oral gavage of vitamin D3 daily significantly improved the body weight gain and immune organ index and significantly reverted the abnormal changes of ALT, AST, SOD, GSH-Px, T-AOC, and MDA in the serum and jejunum induced by diquat. The addition of vitamin D3 also significantly reduced the concentration of DAO, D-LA, and certain proinflammatory cytokines in serum. Moreover, vitamin D3 improved the pathological morphology of the duodenum, jejunum, colon, liver, and kidney tissues, and it also largely attenuated the degree of inflammatory infiltration of macrophages and cell apoptotic index of jejunal epithelial tissue induced by diquat. The results demonstrated that vitamin D3 significantly recovered the intestinal barrier injury by enhancing the expression of mucins and tight junction proteins in the jejunum. In addition, the results indicated that vitamin D3 could significantly reduce the phosphorylation level of NF-κB (p65) and enhance the expression of Nrf2 and HO-1 in the jejunum compared with the diquat-induced group. This study suggested that oral administration of vitamin D3 can protect mice against oxidative damage by inhibiting the phosphorylation level of NF-κB (p65) and activating Nrf2-related signaling pathways.

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“…VDR was also reported to play an important role in gastric mucosa homeostasis and host protection against H. pylori infection ( 13 ). VDR could regulate cathelicidin antimicrobial protein (CAMP) and has an antimicrobial activity against H. pylori ( 13 , 17 ). Past studies found an important role of the VDR/CAMP pathway in innate immunity and an anti-inflammatory mechanism of vitamin D. VDR mRNA expression levels were significantly up-regulated in H. pylori -infected patients and positively correlated with chronic inflammation scores.…”

Section: Introductionmentioning

confidence: 99%

“…VDR knockdown mice were more susceptible to H. pylori infection. In cultured mouse primary gastric epithelial cells, VitD3/VDR complex binds to the CAMP promoter region to increase its expression ( 17 ).…”

Section: Introductionmentioning

confidence: 99%

Comparing the Expressions of Vitamin D Receptor, Cell Proliferation, and Apoptosis in Gastric Mucosa With Gastritis, Intestinal Metaplasia, or Adenocarcinoma Change

et al. 2021

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Background: This study aimed to compare the expression of vitamin D receptor (VDR), cell proliferation, and apoptosis in the gastric mucosa of patients with gastritis, intestinal metaplasia (IM), and adenocarcinoma using artificial intelligence.Material and Methods: This study retrospectively enrolled patients at the Keelung Chang Gung Memorial Hospital from November of 2016 to June, 2017, who were diagnosed with gastric adenocarcinoma. The inclusion criteria were patients' pathologic reports that revealed all compartments of Helicobacter pylori infection, gastritis, IM, and adenocarcinoma simultaneously in the same gastric sample. Tissue slides after immunohistochemical (IHC) staining were transformed into digital images using a scanner and counted using computer software (QuPath and ImageJ). IHC staining included PA1-711 antibody for VDR, Ki67 antigen for proliferation, and M30 antibody CK18 for apoptosis.Results: Twenty-nine patients were included in the IHC staining quantitative analysis. The mean age was 69.1 ± 11.3 y/o. Most (25/29, 86.2%) patients had poorly differentiated adenocarcinoma. The mean expression of Ki67 and CK18 increased progressively from gastritis and IM to adenocarcinoma, with statistical significance (P < 0.05). VDR expression did not correlate with Ki67 or CK18 expression. Survival time was only correlated with tumor stage (correlation coefficient = −0.423, P value < 0.05), but was not correlated with the expression of VDR, Ki67, and CK18.Conclusion: Ki67 expression and CK18 expression progressively increased in the areas of gastritis, IM, and adenocarcinoma. No correlation between VDR expression and Ki67 or CK18 expression was found in this study.

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Vitamin D3 Inhibits Helicobacter pylori Infection by Activating the VitD3/VDR-CAMP Pathway in Mice

Cited by 20 publications

References 44 publications

Impact of Dietary Patterns on H. pylori Infection and the Modulation of Microbiota to Counteract Its Effect. A Narrative Review

Impact of Dietary Patterns on H. pylori Infection and the Modulation of Microbiota to Counteract Its Effect. A Narrative Review

Vitamin D3 Protects Mice from Diquat-Induced Oxidative Stress through the NF-κB/Nrf2/HO-1 Signaling Pathway

Comparing the Expressions of Vitamin D Receptor, Cell Proliferation, and Apoptosis in Gastric Mucosa With Gastritis, Intestinal Metaplasia, or Adenocarcinoma Change

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